Complications of Alcohol
Today in morning report we discussed a patient presenting with worsening peripheral edema and ascites.
This patient has a known history of cirrhosis secondary to alcohol.
It is important when assessing patients to have a framework of the likely causes for why they are presenting today, as well as to consider all of the dangerous complications/consequences of their underlying condition that often plays a role in their presentation. This will also help to shape your history/ddx/communications of the case.
In a patient with cirrhosis, some issues to consider when assessing:
1. Encephalopathy, also remember, think about what has caused their encephalopathy
2. SBP (Spontaneous bacterial peritonitis)
3. GI bleeds, specifically variceal bleeds.
4. Hyponatremia and neurologic sequelae from that.
Back to this patient. When assessed, there was no neurologic symptoms, mental status was normal, no evidence of asterixis. There was no abdominal tenderness, no fevers/chills/sweats. Lastly there was no evidence of melena stools or hematemesis.
Because of his change in clinical status, the question of SBP was raised, and so a diagnostic tap was performed.
A word on SBP:
Changes in clinical status in a patient with cirrhosis essentially warrants a diagnostic tap to ensure that they have not developed SBP. remember that SBP is mono-microbial due to transient bacteremia returning and seeding the ascitic fluid. It is not as previously thought due to GI translocation (if it were, would see polymicrobial infections).
When doing your diagnostic tap, keep the number 250 in your head, which is the cut off of neutrophils below which is sensitive to rule out SBP.
If SBP is suspected, empiric treatment is targeted and enteric organisms and is often a 3rd generation cephalosporin. Additionally, for the treatment of SBP we will use albumin (in the absence of any other contraindications). In 1999 a study in the NEJM looked at ~65 patients in each arm of either cefotaxime or cefotaxime + albumin. Rates of renal impairment, and mortality were approximately 30% in the cefotaxime only arm compared to 10% in the cefotaxime + albumin arm. This gives an ARR of 20% and so a NNT of 5!! Granted was a small study, and the patient population needs to be assessed for whether it applies to your patient. However, this is an oft cited trial to support the use of albumin in SBP.
Last word on the neurologic complications of alcohol:
Acutely and most commonly is the intoxicating effects that alcohol has.
More seriously in the acute setting think about alcohol withdrawal, delirium tremens, Wernicke's. Chronically peripheral neuropathy, midline cerebellar disease, and rarely the marchiafava-bignami syndrome which is disease of the corpus callosum.
See the 1999 NEJM SBP Albumin trial here